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细胞外循环林与CD146结合,对于类风湿性关节炎中Th17细胞分化至关重要

Yuna Zhao¹, Pengtao Jiao², Xiaoyuan Bai³

¹College of Animal Sciences and Veterinary Medicine, Guangxi University, Nanning 530004, Guangxi, China; Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China.

Molecular therapy : the journal of the American Society of Gene Therapy

|October 25, 2025

概括

细胞外环素A (eCypA) 通过促进Th17细胞分化来驱动类风湿性关节炎 (RA). 阻止eCypA与CD146结合,为RA治疗提供了一个有前途的新疗法策略.

科学领域:

免疫学免疫学免疫学
类风湿病学类风湿病学
分子生物学分子生物学

背景情况:

类风湿性关节炎 (RA) 是一种慢性自身免疫性疾病,持续需要新的治疗点.
高细胞外环素A (eCypA) 表达与RA疾病严重程度相关.

研究的目的:

为了研究eCypA在RA病变发生中的作用.
评估抗eCypA单克隆抗体 (mAb) 作为 RA 的潜在治疗策略.

主要方法:

在RA患者中评估eCypA表达.
用抗eCypA mAb治疗的原诱导和原抗体诱导的关节炎小鼠模型.
利用单细胞RNA测序来分析Th17细胞分化.
研究了eCypA-CD146在CD4+T细胞上的相互作用.
在 CD4+ T 细胞中生成条件 CD146 淘汰小鼠.

主要成果:

在小鼠模型中,抗eCypA mAb治疗缓解了关节炎,超过了抗TNF-α治疗.
单细胞RNA测序显示,抗eCypA mAb抑制了STAT3介导的Th17细胞分化.
在CD4+T细胞上与CD146结合的eCypA通过CD146二分化促进了Th17分化.
在CD4+T细胞中,有条件的CD146淘汰抑制了Th17分化,并降低了关节炎的严重程度.

结论:

在RA中,eCypA通过CD146.6驱动Th17细胞的分化.
阻止eCypA-CD146相互作用是一种潜在的类风湿性关节炎治疗方法.

关键词:

CD146 是一个 CD146 是一个 CD146 Th17细胞分化的过程细胞外的环素A.类风湿性关节炎类风湿性关节炎

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